Nominal Zelltoxizit t differentiated E46K after expression in PC12 cells. E46K locked syn proteasome activity t and induces mitochondrial depolarization in the cell model. Baicalein has been reported that wild-type in vitro inhibit Dehydrogenase syn fibrillation, and protect neurons from several chemical models induced parkinsonism. We now recognize that baicalein significantly attenuated Cht E46K-induced mitochondrial depolarization and proteasome inhibition and protected cells from toxicity t, Induced by the E46K in a cellular model of Parkinson’s disease. Baicalein reduces E46K fibrillation also in vitro with a dose–Dependent beta-sheet conformation, although it is obtained oligomeric species Ht, and induces a decrease in the aggregate formation of syn E46K and stored toxicity t N2A cells.
Taken together, these data show that the mitochondrial dysfunction, proteasome inhibition and specific 2-Methoxyestradiol aspects of the abnormal aggregation E46K E46K accompany syn induced Zelltoxizit t and baicalein and protect Modify the properties of aggregation. Baicalein has potential as a tool for reinforcing t Ndnis the relationship between species aggregation and toxicity And may be a candidate compound for further validation with syn in vivo models genetic PD. Introduction of Parkinson’s disease is a progressive neurodegenerative disease that tremor, rigidity and bradykinesia causes postural instability t, autonomic and cognitive and emotional among other cardinal signs. It is due to the loss of dopaminergic neurons in the substantia nigra of the brain and cytoplasmic inclusions as Lewy K rpern Known.
Although there are effective ways to treat the symptoms pers Nlichen motor characteristics of PD, there is no neuroprotective treatment, prevent the progressive loss of dopaminergic neurons. Synuclein is a protein that is localized in the clear function pr Synaptic terminals in the CNS and, together with ubiquitin and synphilin 1, a major component of Lewy K Rperchen in PD. Three syn mutations have been identified to cause familial Re Parkinson. Although the syndrome mutation occurs rarely shows Genetic similarity between the genetic and sporadic forms of PD PD models help us to dissect the most important biochemical pathways and pathogenic PD. He Ffnete genetic forms of Parkinson new avenues for research in PD and St requirements Characterized by the accumulation of syn.
Zus Tzlich appears ver MODIFIED expression of normal syn be a risk factor for sporadic PD. Therefore, the investigation of syn-induced PD pathogenesis not only illuminate the genetic forms of Parkinson’s disease, but also the pathogenesis of sporadic PD aufzukl Ren and has led to the development of drugs therapeutic potential. The E46K mutation was identified after the A30P and A53T mutations, and helped the association of mutations with Parkinson syn family best Term. Patients with dementia with Lewy E46K mutation K rperchen, Parkinson’s disease or PD. Continue to be syn E46K unl-Insoluble fibrils in vitro faster than the wild-type protein. E46K syn shows both a Erh Increase the binding of lipid and filament relative to the wild-type-syn. Electron microscopy showed that E46K syn fibrils have a typical structure extremely Amylo And with syn E46K erh Ht amyloid fibril formation Of. In the culture of ugetierzellen S, Syn E46K tag